UTTAR PRADESH JOURNAL OF ZOOLOGY

The occurrence of skin cancer is increasing worldwide and UV radiation is a critical causative agent, which leads to the initiation and progression of skin cancer. The skin cancers are categorized into melanoma (MSC) and non-melanoma skin cancers (NMSC), in which the former is more dangerous and unable to be treated in advanced conditions. The present study aims to assess the protective role of hypericin in ultraviolet-B (UV-B)- mediated oxidative imbalance and alterations in the protein expression of autophagic markers in the skin of mice. The animals were randomized and grouped (n = 6) into normal, UV-B exposed (180 mJ/cm² for 30 weeks), UV-B + Hypericin (0.1%), UV-B + Hypericin (0.2%), UV-B + Hypericin (0.4%) and Hypericin (0.4%), alone treated. Hypericin was administered topically thrice a week for 30 weeks one hour before radiation exposure. Significant enhancement in TBARS levels and reduction in the levels of GSH and activities of SOD, catalase and GPx were found in UV-B-alone exposed mice, whereas the topical application of hypericin significantly ameliorated the UV-B- mediated oxidative stress and increased the antioxidant levels due to its potent antioxidant property. UV-B radiation exposure diminished the expression of ATG-5, Beclin-1 and LC3-II and enhanced the expression of p62 and LC3-I, thereby suppressing autophagy. The hypericin co-treatment also reversed UV-B-induced alterations in the expression of autophagic markers (ATG-5, Beclin-1, LC3-I, LC3-II and p62), thereby enhancing autophagy and inducing apoptosis. The hypericin co-treatment attenuated these pathological changes due to its anticancer properties. However, more studies are required to evaluate the radioprotective role of hypericin by carrying out more research on the anti-apoptotic and anti-inflammatory effect of hypericin.